Evidence map›Paper›PMID 18670647›Full record

ArticleNeoplasia (New York, N.Y.)2008

Homozygous deletions and recurrent amplifications implicate new genes involved in prostate cancer.

Wennuan Liu, Chunmei Carol Xie, Yi Zhu, Tao Li, Jishan Sun, Yu Cheng, Charles M Ewing, Sue Dalrymple, Aubrey R Turner, Jielin Sun and 5 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
7.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

72 citing papers in PubMed, 126 citations in OpenAlex.

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12 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 2 institutions in 1 country.

Wennuan LiuCenter for Cancer Genomics, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Chunmei Carol Xie
Yi Zhu
Tao Li
Jishan Sun
Yu Cheng
Charles M Ewing
Sue Dalrymple
Aubrey R Turner
Jielin Sun
John T Isaacs
Bao-Li Chang
Siqun Lilly Zheng
William B Isaacs
Jianfeng Xu
Wake Forest University · USJohns Hopkins University · US

Funding

Association of inflammatory genes and prostate cancerR01CA105055 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI XU, JIANFENG · 2004 to 2008
$2.4M
Interaction of PTEN and CDKN1B in Pca susceptibilityR01CA106523 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI XU, JIANFENG · 2004 to 2008
$1.6M
Mapping Prostate Cancer Susceptibility Genes at 8p22-23R01CA095052 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI XU, JIANFENG · 2003 to 2007
$1.4M
NCI NIH HHS CA105055NCI NIH HHS CA106523NCI NIH HHS CA95052NCI NIH HHS PC051264NCI NIH HHS R01 CA095052NCI NIH HHS R01 CA105055NCI NIH HHS R01 CA106523
6 · The paper itself

Abstract

Prostate cancer cell lines provide ideal in vitro systems for the identification and analysis of prostate tumor suppressors and oncogenes. A detailed characterization of the architecture of prostate cancer cell line genomes would facilitate the study of precise roles of various genes in prostate tumorigenesis in general. To contribute to such a characterization, we used the GeneChip 500K single nucleotide polymorphic (SNP) array for analysis of genotypes and relative DNA copy number changes across the genome of 11 cell lines derived from both normal and cancerous prostate tissues. For comparison purposes, we also examined the alterations observed in the cell lines in tumor/normal pairs of clinical samples from 72 patients. Along with genome-wide maps of DNA copy number changes and loss of heterozygosity for these cell lines, we report previously unreported homozygous deletions and recurrent amplifications in prostate cancers in this study. The homozygous deletions affected a number of biologically important genes, including PPP2R2A and BNIP3L identified in this study and CDKN2A/CDKN2B reported previously. Although most amplified genomic regions tended to be large, amplifications at 8q24.21 were of particular interest because the affected regions are relatively small, are found in multiple cell lines, are located near MYC, an oncogene strongly implicated in prostate tumorigenesis, and are known to harbor SNPs that are associated with inherited susceptibility for prostate cancer. The genomic alterations revealed in this study provide an important catalog of positional information relevant to efforts aimed at deciphering the molecular genetic basis of prostate cancer.

Indexed as

Gene DeletionCell Line, TumorChromosomes, Human, Pair 8DNA, NeoplasmGene AmplificationGene Expression ProfilingGenotypeHomozygoteHumansIn Situ Hybridization, FluorescenceLoss of HeterozygosityMaleMembrane ProteinsPolymerase Chain ReactionPolymorphism, Single NucleotideProstatic NeoplasmsBNIP3L protein, humanDNA, NeoplasmMembrane ProteinsPPP2R2A protein, humanProtein Phosphatase 2Proto-Oncogene ProteinsTumor Suppressor Proteins

Identifiers

PMID18670647
PMCPMC2481576
OpenAlexW1547654062

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.